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作 者:Xian Jiang Li Li Zhengxin Ying Chenjie Pan Shaoqiang Huang Lin Li Miaomiao Dai Bo Yan Ming Li Hui Jiang She Chen Zhiyuan Zhang 王晓东
机构地区:[1]不详 [2]北京生命科学研究所 [3]美国国家科学院 [4]中国科学院
出 处:《科学新闻》2017年第4期86-86,共1页Science News
基 金:科技部;北京市政府资助
摘 要:细胞凋亡的刺激会使得哺乳动物细胞中的线粒体释放细胞色素c和其他凋亡蛋白,导致胱天蛋白酶的激活和细胞死亡。Bcl-2蛋白家族的促凋亡成员如Bim和Bax可促进这一过程,Bim和Bax分别从线粒体启动和执行细胞色素c释放。In response to apoptotic stimuli, mitochondria in mammalian cells release cytochrome c and other apoptogenic proteins, leading to the subsequent activation of caspases and apoptotic cell death. This process is promoted by the pro-apoptotic members of the Bcl-2 family of proteins, such as Bim and Bax, which, respectively, initiate and execute cytochrome c release from the mitochondria. Here we report the discovery of a small molecule that efficiently blocks Bim-induced apoptosis after Bax is activated on the mitochondria. The cellular target of this small molecule was identified to be the succinate dehydrogenase subunit B (SDHB) protein of complex II of the mitochondrial electron transfer chain (ETC). The molecule protects the integrity of the ETC and allows treated cells to continue to proliferate after apoptosis induction. Moreover, this molecule blocked dopaminergic neuron death and reversed Parkinson-like behavior in a rat model of Parkinson's disease.
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